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Updated: Sep 3, 2025
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Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
Published on: June 7, 2016
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Angiotensin-(1-9) in hypertension.
Ignacio Norambuena-Soto1, Camila Lopez-Crisosto1, Javiera Martinez-Bilbao1
1Advanced Center for Chronic Diseases (ACCDiS), Faculty of Chemical & Pharmaceutical Sciences and Faculty of Medicine, University of Chile, Santiago, Chile.
Biochemical Pharmacology
|July 23, 2022
Summary
Angiotensin-(1-9) [Ang-(1-9)] effectively lowers blood pressure and reduces organ damage in hypertension models. This peptide activates the angiotensin II receptor type 2 (AT2R), showing promise as an antihypertensive therapy.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Endocrinology
Background:
- The non-canonical renin-angiotensin system (RAS) includes Angiotensin-(1-9) [Ang-(1-9)], synthesized by angiotensin-converting enzyme type 2 (ACE2).
- Ang-(1-9) acts as an endogenous ligand for the angiotensin II receptor type 2 (AT2R).
Purpose of the Study:
- To investigate the antihypertensive and organ-protective effects of Ang-(1-9).
- To explore the role of Ang-(1-9) in activating AT2R and its downstream signaling pathways.
Main Methods:
- Infusion of Ang-(1-9) using osmotic minipumps in rat hypertension models.
- Assessment of blood pressure reduction and hypertension-induced end-organ damage.
- Review of evidence linking Ang-(1-9) to AT2R activation and synthetic AT2R agonists.
Main Results:
- Consistent reduction in blood pressure observed in multiple rat hypertension models following Ang-(1-9) infusion.
- Decreased hypertension-induced end-organ damage in animals treated with Ang-(1-9).
- Evidence suggests Ang-(1-9) is the natural ligand for AT2R, which mediates these protective effects.
Conclusions:
- Angiotensin-(1-9) demonstrates significant potential as an antihypertensive agent by reducing blood pressure and mitigating end-organ damage.
- While synthetic AT2R agonists have been explored, Ang-(1-9) remains a promising therapeutic candidate, though further clinical research is necessary.
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